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Rheumatology
Published in Shibley Rahman, Avinash Sharma, MRCP Part 2 Best of Five Practice Questions, 2018
Shibley Rahman, Avinash Sharma
Which of the following clinical features is unusual in adult onset Still’s disease? arthralgialung fibrosisfeverpericarditissplenomegaly
Unexpectedly lower proportion of placental transferred tocilizumab relative to whole immunoglobulin G: a case report
Published in Scandinavian Journal of Rheumatology, 2020
M Moriyama, Y Wada, T Minamoto, M Kondo, M Honda, Y Murakawa
TCZ is an IgG1 monoclonal antibody that can be transferred to the foetus via the neonatal Fc receptor on the placenta after the second trimester, similarly to other IgG1-type biologics such as adalimumab and infliximab. The median levels of infliximab and adalimumab in the cord are 160% and 153%, respectively, of those in the mother (7). In our case, although the IgG level in the cord was 145% of that in the mother’s serum, the concentration of TCZ in the cord was unexpectedly only 7.6% of that in the mother’s serum at delivery. During the preparation of this report, another group published a case report of adult-onset Still’s disease, with similar observations (6). Therefore, this is the second report to demonstrate a lower proportion of placental transport of TCZ. However, our case is still important in confirming that the relatively low level of TCZ placental transport is a common characteristic of TCZ.
Efficacy and safety of tocilizumab with inhibition of interleukin-6 in adult-onset Still’s disease: A meta-analysis
Published in Modern Rheumatology, 2018
Yubo Ma, Meng Wu, Xu Zhang, Qing Xia, Jiajia Yang, Shengqian Xu, Faming Pan
Adult-onset Still’s disease (AOSD) is an uncommon systemic inflammatory disorder characterized by a number of clinical manifestations: high spiking fever, evanescent maculopapular rash, polyarthritis or arthralgia, lymphadenopathy, elevated acute phase reactants, and other systemic symptoms [1–3]. AOSD is considered as a complex auto-inflammatory syndrome, triggered by infectious agents, genetic factors, and environmental factors, but the exact etiology is still unclear [1,4–7]. Meanwhile, the treatment strategy of AOSD is empirical and merely depends on evidence of case reports and case series [8]. The nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids are first-line medications for AOSD, with the response rate of 60% by combination therapy [2,9]. And high dose of corticosteroid at disease onset usually induces fast remissions and less relapses [9–11]. Disease-modifying anti-rheumatic drugs (DMARDs) and immunosuppressive medicines will then be applied when previous therapy is frustrated [8,12,13]. Nevertheless, corticosteroids often bring about steroid dependence and long-term side effects about in 40–50% individuals, especially infection [8,14]. Hence, there is an impending need for optional therapy to command the manifestations and taper the dose of corticosteroids for patients; fortunately, the emergence of biologics, targeting pro-inflammatory cytokines, gives light to it.
Clinical practice guidance for juvenile idiopathic arthritis (JIA) 2018
Published in Modern Rheumatology, 2019
Nami Okamoto, Shumpei Yokota, Syuji Takei, Yuka Okura, Tomohiro Kubota, Masaki Shimizu, Tomo Nozawa, Naomi Iwata, Hiroaki Umebayashi, Noriko Kinjo, Tomoko Kunishima, Junko Yasumura, Masaaki Mori
Systemic JIA is considered to be an autoinflammatory disorder in a broad sense. It is accompanied by intermittent systemic inflammation arising from abnormal innate immunity and overproduction of inflammatory cytokines such as interleukin (IL)-1, IL-6 and IL-18, which is closely associated with the clinical condition [11]. As systemic JIA progresses, hypercytokinemia (cytokine storm) may occur and patients may then present with symptoms of macrophage activation syndrome (MAS), as described below (see Section 7). Although there are only a few reports, recent studies reveal similar clinical characteristics as in adult-onset Still’s disease in terms of the cytokine profile and response to treatment [12].